Abstract

The mechanism that alters the pulmonary VO2 response to heavy-intensity exercise following prior heavy exercise has been frequently ascribed to an improvement in pre-exercise blood flow (BF) or O(2) delivery. Interventions to improve O(2) delivery have rarely resulted in a similar enhancement of VO2. However, the actual limb blood flow and VO2 dynamics in the second bout of repeated exercise remain equivocal. Seven healthy female subjects (21-32 years) performed consecutive 6-min (separated by 6 min of 10 W exercise) bilateral knee extension (KE) exercise in a semisupine position at a work rate halfway between the lactate threshold (LT) and VO2peak. Femoral artery blood flow (FBF) was measured by Doppler ultrasound simultaneously with breath-by-breath VO2 each protocol being repeated at least four times for precise kinetic characterization. The effective time-constant (tau') of the VO2 response was reduced following prior exercise (bout 1: 61.0 +/-10.5 vs. bout 2: 51.6+/-9.0 s; mean +/- SD; P<0.05), which was a result of a reduced slow component (bout 1: 16.0+/-8.0 vs. bout 2: 12.5+/-6.7 %; P<0.05) and an unchanged 'primary' tau. FBF was consistently faster than VO2. However, there was no bout-effect on tau' FBF (bout 1: 28.2+/-12.0 vs. bout 2: 34.2+/-8.5 s). The relationship between the exercise-associated VO2 (i.e., deltaVO2) and Delta FBF was similar between bouts, with a tendency (N.S: P>0.05) for deltaVO2/deltaFBF to be increased during the transition to bout 2 rather than decreased, as hypothesized. The return of VO2 kinetics toward first order, therefore, was associated with an 'appropriate', not enhanced, BF to the working muscles. Whether a relative prior-hyperemia in bout 2 enables a more homogeneous intramuscular distribution of BF and/or metabolic response is unclear, however, these data are consistent with events more proximal to the exercise muscle in mediating the VO2 response during repeated heavy-intensity KE exercise.

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